1. Cardiogenic shock complicating acute myocardial infarction—etiologies,
management and outcome: a report from the SHOCK Trial Registry
Judith S. Hochman, Christopher E. Buller, Lynn A. Sleeper, Jean Boland, Vladimir
Dzavik, Timothy A. Sanborn, Emilie Godfrey, Harvey D. White, John Lim, Thierry
LeJemtel, for the SHOCK Investigators
J. Am. Coll. Cardiol. 2000;36;1063-1070
This information is current as of January 12, 2010
The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http://content.onlinejacc.org/cgi/content/full/36/3_Suppl_A/1063
Downloaded from content.onlinejacc.org by on January 12, 2010

2. Journal of the American College of Cardiology Vol. 36, No. 3, Suppl A
© 2000 by the American College of Cardiology ISSN 0735-1097/00/$20.00
Published by Elsevier Science Inc. PII S0735-1097(00)00879-2
Cardiogenic Shock Complicating Acute Myocardial
Infarction—Etiologies, Management and
Outcome: A Report from the SHOCK Trial Registry
Judith S. Hochman, MD, FACC,* Christopher E. Buller, MD, FACC,† Lynn A. Sleeper, SCD,‡
Jean Boland, MD,§ Vladimir Dzavik, MD, Timothy A. Sanborn, MD, FACC,¶
Emilie Godfrey, MS, RD,* Harvey D. White, DSC, FACC,# John Lim, BA,‡ Thierry LeJemtel, MD,**
for the SHOCK Investigators
New York, New York; Vancouver and Edmonton, Canada; Watertown, Massachusetts; Liege, Belgium;
Auckland, New Zealand
OBJECTIVES This SHOCK Study report seeks to provide an overview of patients with cardiogenic shock
(CS) complicating acute myocardial infarction (MI) and the outcome with various treat-
ments. The outcome of patients undergoing revascularization in the SHOCK Trial Registry
and SHOCK Trial are compared.
BACKGROUND Cardiogenic shock is the leading cause of death in patients hospitalized for acute MI. The
randomized SHOCK Trial reported improved six-month survival with early revasculariza-
tion.
METHODS Patients with CS complicating acute MI who were not enrolled in the concurrent randomized
trial were registered. Patient characteristics were recorded as were procedures and vital status
at hospital discharge.
RESULTS Between April 1993 and August 1997, 1,190 patients with CS were registered and 232 were
randomized in the SHOCK Trial. Predominant left ventricular failure (78.5%) was most
common, with isolated right ventricular shock in 2.8%, severe mitral regurgitation in 6.9%,
ventricular septal rupture in 3.9% and tamponade in 1.4%. In-hospital Registry mortality was
60%, with ventricular septal rupture associated with a significantly higher mortality (87.3%)
than all other categories (p 0.01). The risk profile and mortality were lower for Registry
patients who were managed with thrombolytic therapy and/or intra-aortic balloon counter-
pulsation, coronary angiography, angioplasty and/or coronary artery bypass surgery. After
adjusting for these differences, the extent to which survival was improved with early
revascularization was similar to that observed in the randomized SHOCK Trial.
CONCLUSIONS In this prospective Registry the etiology of CS was a mechanical complication in 12%. The
similarity of the beneficial treatment effect in patients undergoing early revascularization in
the SHOCK Trial Registry and SHOCK Trial provides strong support for the generaliz-
ability of the SHOCK Trial results. (J Am Coll Cardiol 2000;36:1063–70) © 2000 by the
American College of Cardiology
Over the past 15 years, 30-day mortality and overall Nonrandomized studies have reported a reduced mortal-
complications of acute myocardial infarction (MI) have ity rate for patients with CS undergoing revascularization
been substantially reduced by the use of reperfusion therapy (5–10). A recently reported international randomized trial,
(1–3). However, cardiogenic shock (CS) remains the lead- SHould we emergently revascularize Occluded Coronaries
ing cause of death in patients hospitalized with acute MI for cardiogenic shocK? (the SHOCK Trial), was supported
(4). Thrombolytic therapy alone has had a limited effect on by the National Heart, Lung, and Blood Institute. The
the outcome of patients presenting with pump failure (1,3). SHOCK Trial assessed the effects on 30-day mortality of a
Further insights into the mechanisms of shock and the direct invasive strategy (emergency early coronary angiog-
outcomes of various treatment modalities currently in use raphy and revascularization), compared with a strategy of
are needed to substantially alter the high mortality rate of initial medical stabilization (including thrombolysis and
intra-aortic balloon counterpulsion [IABP]) followed by
CS.
delayed mechanical revascularization as clinically deter-
mined (11). Concurrent with this randomized trial, data
From *St. Luke’s–Roosevelt Hospital Center and Columbia University, New York, have also been collected on patients with suspected CS
New York; †Vancouver Hospital & Science Center, Laurel Cardiology, Vancouver, complicating acute MI who were not randomized at the 36
British Columbia, Canada; ‡New England Research Institutes, Watertown, Massa- participating institutions. This Registry of the SHOCK
chusetts; §CHR Citadelle, Department of Cardiology, Liege, Belgium; University of
Alberta, Div. of Cardiology, Edmonton, Canada; ¶New York Cornell Medical Trial offers a unique opportunity to: 1) further define the
Center, New York, New York;# Green Lane Hospital, Auckland, New Zealand; mechanisms responsible for CS in patients with acute MI,
**Albert Einstein Medical Center (College of Medicine), New York, New York. 2) review the utilization rates of therapeutic modalities and
Supported by grants from the National Heart, Lung and Blood Institute (RO1-
HL50020-018Z and RO1-HL49970.) their impact on mortality, and 3) compare the effect of early
Manuscript received February 16, 2000, accepted March 17, 2000. revascularization on mortality in both the Registry and Trial
Downloaded from content.onlinejacc.org by on January 12, 2010

3. 1064 Hochman et al. JACC Vol. 36, No. 3, Suppl A
CS Complicating Acute MI September 2000:1063–70
(for non-anterior MI) or pulmonary congestion on a chest
Abbreviations and Acronyms X-ray, with subsequent hemodynamic confirmation (for
CK creatine kinase anterior MI). Moreover, only patients with CS due to
CS cardiogenic shock predominant LV failure with ECG evidence of recent total
LBBB left bundle branch block
coronary occlusion, e.g., ST elevation, Q waves, new left
LV left ventricular, left ventricle
MI myocardial infarction bundle branch block (LBBB) or posterior MI with anterior
MR mitral regurgitation ST depression, were eligible for the trial.
PCWP pulmonary capillary wedge pressure Enrollment in the SHOCK Trial Registry, however,
RV right ventricular, right ventricle which forms the basis for the current report, required only
SHOCK SHould we emergently revascularize
Occluded Coronaries for cardiogenic shocK? that CS be suspected on clinical grounds. Etiologies of CS
VSR ventricular septal rupture other than predominant LV failure (e.g., acute severe mitral
regurgitation [MR], ventricular septal rupture [VSR], iso-
lated right ventricular [RV] failure, cardiac tamponade or
cohorts. This report provides an overview of the entire rupture, prior severe valvular heart disease, excess beta or
SHOCK study. In-depth analyses of the major etiologies of calcium channel blockade, dilated cardiomyopathy, and CS
shock, and the various treatment modalities, are presented associated with recent hemorrhage or cardiac catheteriza-
in other reports in this supplementary issue of the Journal. tion laboratory complication) constituted clinical exclusion
Enrollment in the SHOCK Trial Registry and SHOCK criteria in the SHOCK Trial, and patients with such
Trial started in April 1993 and was completed for the etiologies were entered into the SHOCK Trial Registry.
Registry on August 31, 1997, and for the Trial on Novem- Patients with VSR or acute severe MR without CS were not
ber 30, 1998. Eleven hundred and ninety patients were registered, because the diagnosis of suspected CS was
enrolled in the SHOCK Trial Registry, and 232 patients required. Patients with any etiology of CS whose course was
were enrolled in the SHOCK Trial as of August 31, 1997. outside the time windows of CS 36 h after MI and
This is the largest body of experience prospectively collected randomization 12 h after shock diagnosis were also
to date relating to unselected patients with CS complicating included in the SHOCK Trial Registry.
acute MI. Data from the 302 patients enrolled in the randomized
SHOCK Trial between April 1993 and November 1998
METHODS (11) are presented: 1) to assess the effect of revascularization
on mortality in the SHOCK Trial Registry, compared to
Patient sample. One thousand one hundred ninety pa-
the SHOCK Trial, and 2) to assess the incidence of major
tients with suspected CS complicating acute MI were
etiologies of shock for all screened (Registry and Trial)
prospectively registered. A local discharge diagnosis of acute
MI and CS (DRG’s 410 and 785.51) or a suspected patients. For the latter analysis, we included only the 232
diagnosis of CS complicating acute MI, regardless of the predominant LV failure patients enrolled in the Trial as of
final discharge diagnosis, constituted the criteria for registry August 31, 1997, the time period concurrent with Registry
enrollment. enrollment. Mortality rates for the major shock etiologies
Thirty-six centers were initiated in a staggered fashion, are presented for: 1) all Registry patients, 2) the predomi-
with the first patient enrolled in April 1993. Seven hundred nant LV failure cohort within the Registry and 3) the
and thirty patients (61%) were registered in 24 U.S. centers, Registry and concurrent Trial patients combined.
256 (22%) in five Canadian centers, 76 (6%) in four Belgian Data collection. Data were abstracted from the medical
centers and 128 (11%) in Australia, New Zealand and record by the SHOCK study coordinators, who were
Brazil. All centers obtained Institutional Review Board or centrally trained to complete standardized study report
Ethics Committee approval for the abstraction of medical forms. Patient characteristics, MI characteristics, hemody-
records. namics, medication and procedure utilization, and vital
Enrollment in the SHOCK Trial Registry rather than the status at hospital discharge were recorded.
randomized SHOCK Trial occurred if a patient with Definitions. Predominant LV failure was designated as the
suspected CS failed to meet all trial inclusion criteria or etiology of CS when none of the other following major
specified time windows, met a trial exclusion criterion, or shock categories was indicated as present: isolated RV
was unable or refused to give consent. As previously shock, mechanical cause (acute severe MR, VSR, or tam-
reported (12), the criteria for CS for the randomized ponade/LV rupture), prior severe valvular heart disease,
SHOCK Trial consisted of: 1) hypotension (systolic blood excess beta or calcium channel blockade, or shock resulting
pressure 90 mm Hg for at least 30 min, need for from a cardiac catheterization laboratory complication.
vasopressors, or IABP support); 2) clinical evidence of end ECG locations were defined as follows (GUSTO I) (13):
organ hypoperfusion; and 3) confirmatory hemodynamic or
V1 V 4 Anterior; II, III, AVF Inferior;
radiographic features: pulmonary capillary wedge pressure
(PCWP) 15 mm Hg and cardiac index 2.2 l/min/m2 V5 V 6 Apical; I, AVL Lateral; V 1 V 2 Posterior.
Downloaded from content.onlinejacc.org by on January 12, 2010

4. JACC Vol. 36, No. 3, Suppl A Hochman et al. 1065
September 2000:1063–70 CS Complicating Acute MI
Reinfarction was defined as follows: 1) recurrent chest pain Table 1. Registry Patient Characteristics
or ischemic symptoms 30 min and recurrent ST-segment All Predominant Other
elevation, new Q waves, or new LBBB; 2) total creatine Patients LV Failure Categories
kinase (CK) at least twice the upper limit of normal and n 1,190 884 306
25% or 200 U/mL over the previous value, with an Age (yrs) 68.7 11.8 68.5 12.1 69.5 11.1
elevated CK-MB level; or 3) a rise in CK-MB above the Male (%) 59.7 63.6 48.3*
upper limit of normal after it had reverted to the normal White, non- 82.0 83.6 77.4**
Hispanic (%)
range.
History of MI (%) 37.4 40.1 29.5***
Hemodynamic data. Right heart catheterization was per- History of hypertension (%) 53.1 51.7 57.2
formed in 790 Registry patients, with PCWP recorded in Diabetes (%) 32.6 32.8 32.0
739 patients and cardiac index in 562 patients. Left ven- Smoker (%) 50.1 51.5 45.9
tricular (LV) ejection fraction was measured at any time History of elevated lipids 41.8 40.2 46.4
(%)
during the hospitalization in 468 patients, by LV angiog-
History of renal 10.9 10.7 11.6
raphy (37%), gated blood pool scan (4%) or echocardiogra- insufficiency (%)
phy (59%). Hemodynamic measurements included those History of PTCA (%) 6.2 6.7 4.8
recorded while the patient was receiving supportive therapy. History of CABG (%) 9.6 10.1 8.1
Statistical methods. The characteristics of patients with Other severe illness (%) 18.1 17.7 19.4
History of peripheral 17.9 18.8 15.4
predominant LV failure versus other causes of shock were
vascular disease (%)
compared using the Fisher exact test for categorical vari-
*p 0.0001 vs. LV failure; **p 0.019 vs. LV failure; ***p 0.001 vs. LV failure.
ables, the Wilcoxon rank-sum test for ordinal and non-
normally distributed continuous variables, and Student
t-test for normally distributed continuous variables. Median Major shock categories. The incidences of the major
values are presented with 25th and 75th percentiles, and categories of shock were assessed. Predominant LV failure
means with standard deviation. In six patients there were caused CS in 78.5% of all (Registry and Trial, n 1,422)
multiple causes of shock, and for the purposes of compari- cases. Acute severe MR was diagnosed in 98 (6.9%), VSR in
son of mortality rates these patients were categorized as 55 (3.9%), isolated RV shock in 40 (2.8%), tamponade/
having one cause based on the following hierarchical rank- rupture in 20 (1.4%) and other causes (as defined in the
ing: 1) predominant LV failure, 2) VSR, 3) severe MR, 4) Methods section) in 95 (6.7%) (Fig. 1). Six patients fell into
isolated RV failure, 5) cardiac tamponade and 6) other cause more than one category (see the Methods section), and four
of shock. The p values reported for the comparisons of these patients could not be categorized.
groups are unadjusted for multiple comparisons. Four pa- MI characteristics of Registry patients. Multiple-site in-
tients are included in the overall mortality analysis; but the farct locations were often noted on ECG (50%). Anterior
etiology of shock was unknown, and these patients are not MI was diagnosed in 55%, inferior in 46%, posterior in 19%,
included in any shock subgroup. Logistic regression was lateral in 32%, apical in 11% and unknown in 10%.
used to model mortality (dead vs. alive) of patients with Electrocardiographic evidence of ST elevation and/or Q
predominant LV failure by revascularization status, with waves or new LBBB MI was present in 79.1%. Median time
adjustment for factors associated with selection for revascu- from MI to shock was 7.0 h (25th to 75th percentile, 1.8 to
larization. Forty-one patients were excluded from modeling, 22.0). The highest creatine phosphokinase was elevated a
because the revascularization attempt occurred before shock median of 8.4 times (25th to 75th percentile, 2.9 to 18.6)
onset. Models, including cardiac index as a covariate, were above the upper limit of normal. Recurrent MI and recur-
restricted (by definition) to patients undergoing right heart rent ischemia occurred between the initial MI associated
catheterization, approximately half of all predominant LV with hospital admission and shock in 9.3% and 19.7% of
failure patients. All analyses were conducted using the patients, respectively, and were associated with hypotension
Statistical Analysis System (SAS Institute; Cary, North in 86.1% and 69.5%, respectively.
Carolina). Hemodynamics and pharmacologic support. The hemo-
Results. Eleven hundred and ninety patients were regis- dynamic values for all Registry patients, including those
tered as of August 31, 1997, the closing date of the with predominant LV failure causing CS (Table 2), were
SHOCK Trial Registry database. The SHOCK Trial ran- most often recorded after support measures (IABP and/or
domized 232 patients with predominant LV failure during vasopressors) were instituted. For the 790 who underwent
the concurrent period of April 1993 through August 1997 right heart catheterization, the range of cardiac index and
and an additional 70 patients as of the completion of Trial PCWP was broad. Pharmacologic support included vaso-
enrollment on November 30, 1998. Characteristics of the pressors in 95.1% (dopamine 89.3%, norepinephrine 31.6%,
patients in the Registry are shown in Table 1. The mean age epinephrine 41.9%) and/or dobutamine in 70.1%.
was 68.7 11.8 years, and 40.3% were women. There were Predominant LV failure. In the Registry group with
high rates of history of MI, hypertension, diabetes and predominant LV failure (n 884), patients were more
smoking. likely to have had prior MI (40.1% vs. 29.5%, p 0.001)
Downloaded from content.onlinejacc.org by on January 12, 2010

5. 1066 Hochman et al. JACC Vol. 36, No. 3, Suppl A
CS Complicating Acute MI September 2000:1063–70
Figure 1. The complete population of all shock patients screened, including 1,190 Registered patients and 232 Trial patients randomized concurrent with
the Registry from 4/93 – 8/97, is represented in the figure. Of the 1,116 patients with LVF, 844 were Registry and 232 were Trial. The mortality rates
for the 1,190 Registry patients and 884 LVF Registry patients are 61.4% and 60.8%, respectively. The incidence (%, below each bar) and mortality for the
major shock categories is shown. LVF predominant LV failure (see Methods section), RVF isolated RV shock, MR acute severe mitral
regurgitation, VSR ventricular septal rupture, Tamp cardiac tamponade/rupture. Other causes are described in the methods section. The categorization
of cardiogenic shock was unknown in four patients who had a 75% mortality rate. Between group comparisons are based on hierarchical groups in order
from left to right. Six patients fell into more than one category (see text).
and to be white (83.6% vs. 77.4%, p 0.019), compared concurrent Trial combined) rate of 60.1%. The rates were
with patients in the other shock categories (Table 1). significantly different among the six etiologies. Ventricular
Women represented a smaller proportion of the Registry septal rupture patients had higher mortality (87.3%) than
patients with predominant LV failure, compared with the those with predominant LV failure (p 0.0002), RV shock
other shock categories (36.4% vs. 51.7%, p 0.0001). (p 0.002), MR (p 0.0001), as well as every other
Otherwise, there were no significant differences in the category (p 0.01). The mean in-hospital LV ejection
patient characteristics of those with predominant LV failure fraction of 257 Registry survivors was significantly higher
compared to those in the other shock categories. Among than that of 211 nonsurvivors (34.3 13.7% vs. 30.4
LV failure patients, anterior MI location on ECG was most 13.7%, p 0.002). Within the predominant LV failure
common (58.8%), although 34.4% had inferior MI without subgroup, the mean LV ejection fraction for 196 survivors
anterior involvement. Of the latter, 100 (38.3%) had a prior was higher than that of 143 nonsurvivors (32.9 12.8 % vs.
MI. Therefore, 21.2% of those with predominant LV failure 27.4 11.7%, p 0.0001). Registry patients who were
had a first inferior MI with no anterior involvement. Over transferred (44%) to the SHOCK Trial tertiary care center
half of this subgroup (53.4%) had lateral, posterior and/or had a markedly lower mortality than direct admissions
apical involvement on ECG. (56%) to those centers (54% vs. 67%, p 0.001).
Mortality. In-hospital mortality for the major shock cate-
Procedure utilization and outcome for Registry patients
gories is shown in Figure 1, with an overall (Registry and
with predominant LV failure. Registry patients were clin-
Table 2. Hemodynamic Profile of Registry Patients*
ically selected (not randomized) to undergo different treat-
ments, which were not mutually exclusive. Thrombolytic
All Registry Predominant therapy was administered in 36%, while IABP was placed in
Patients LV Failure
(n 1,190) (n 884) 53%. Thrombolytic therapy alone (15%), IABP use alone
n Mean SD N Mean SD
(33%), and thrombolytic therapy with IABP use (20%) were
Systolic BP (mm Hg) 1,124 87.7 22.3 833 88.4 23.0 each associated with lower mortality than no IABP or no
Diastolic BP (mm Hg) 976 52.3 17.0 729 52.7 17.2 thrombolytic therapy use (32%) (62.9%, 52.6%, 46.5% vs.
Heart rate (mm Hg) 1,121 95.7 26.2 832 95.2 25.8 76.5% in-hospital mortality, respectively, p 0.005).
PCWP (mm Hg) 739 23.4 8.4 534 23.7 8.6
Left heart cardiac catheterization with coronary angiog-
Cardiac index (1/min/m2) 562 2.08 0.77 408 2.06 0.78
PA systolic (mm Hg) 482 41.2 12.8 341 41.1 12.8 raphy and revascularization performed at any time during
PA diastolic (mm Hg) 484 23.6 7.8 343 23.8 8.0 the hospitalization are shown in Figure 2. Also shown are
LV ejection fraction (%) 468 32.6 13.8 339 30.6 12.6 in-hospital mortality rates for patients undergoing early
*Measurements were most often obtained on support measures; sympathomimetic percutaneous transluminal coronary angioplasty (PTCA) or
amines and/or intra-aortic balloon counterpulsation
BP Blood pressure; LV Left ventricular; PA Pulmonary artery; PCWP
coronary artery bypass graft surgery (CABG) within 18 h of
Pulmonary capillary wedge pressure. shock diagnosis. This timing of revascularization corre-
Downloaded from content.onlinejacc.org by on January 12, 2010

6. JACC Vol. 36, No. 3, Suppl A Hochman et al. 1067
September 2000:1063–70 CS Complicating Acute MI
Figure 2. Patients with predominant LV failure clinically selected to undergo left heart catheterization and coronary angiography (LH cath) had a lower
mortality than those with no LH cath. Patients with no revascularization attempt had higher mortality, with the lowest mortality observed in patients
selected to undergo CABG. The CABG group includes 18 patients who underwent CABG post-PTCA; these patients are not included in the PTCA
group. The mortality rates for those undergoing early revascularization (within 18 h of shock diagnosis), at a time comparable to the randomized SHOCK
Trial, are shown. The median times to PTCA and CABG are 2.8 and 3.9 h, respectively, for those revascularized 18 h post-shock.
*Patients with PTCA or CABG prior to shock are excluded.
sponds to the upper time limit for early revascularization 0.005), and more often had CS diagnosis within 6 h of MI
after shock in the SHOCK Trial. Left ventricular assist (48.2% vs. 39.6%, p 0.02). The odds ratio (OR) for death,
devices were used in 0.8% (based on 856 with available after adjusting for selection factors, for patients undergoing
data). Performance of coronary angiography, PTCA, and PTCA or CABG, compared with those without revascu-
CABG were each associated with lower in-hospital mortal- larization, is shown in Table 3. The effect of revasculariza-
ity rates than in patients managed without these treatments tion observed in the SHOCK Trial was obtained by
(Fig. 2). Reports on IABP and thrombolysis (14), and comparing all trial patients undergoing a revascularization
angiographic findings (15), appear in this supplementary attempt at any time during hospitalization with those who
issue of the Journal. did not (without regard to group assignment). The OR for
Registry patients undergoing PTCA and CABG at any death with revascularization in the SHOCK Trial was 0.35,
time during the shock hospitalization were younger (64.2 similar to the adjusted OR of 0.30 observed in the SHOCK
11.6 vs. 72.0 11.3 years, p 0.0001), had a lower Trial Registry cohort. Table 4 summarizes the impact of
incidence of prior MI (35.3% vs. 44.2%, p 0.009), revascularization within 18 h of CS, compared with no or
diabetes (28.2% vs. 36.7%, p 0.009), and prior CHF late revascularization. In this analysis Trial patients were
(12.8% vs. 25.7%, p 0.0001), and a higher cardiac index grouped according to their assigned treatment strategy
(2.2 0.8 vs. 1.9 0.7 l/min/m2, p 0.001) and LV because the upper time limit for early revascularization was
ejection fraction (32.1 12.4 % vs. 28.5 12.7 %, p 18 h (12). The adjusted OR for death with early revascu-
Table 3. Effect of Revascularization on Mortality
Odds Ratio for Death Revascularization vs. No Revascularization
Odds
n Ratio 95% CI Comments
Trial 302 0.35 0.22, 0.55 170 underwent a
(30-Day mortality)* revascularization attempt
vs. 132 who did not
undergo revascularization†
Registry 800 0.18 0.13, 0.25 Unadjusted
(In-hospital mortality) 800 0.22 0.16, 0.30 Adjusted for age, diabetes,
MI to CS 6 h
389 0.30 0.19, 0.47 Adjusted for cardiac index,
age, diabetes, prior MI
*Trial in-hospital and 30-day mortality were similar. †Revascularization was performed at any time during the hospitalization
and includes all revascularized patients without regard to trial group assignment (11).
CI Confidence interval.
Downloaded from content.onlinejacc.org by on January 12, 2010

7. 1068 Hochman et al. JACC Vol. 36, No. 3, Suppl A
CS Complicating Acute MI September 2000:1063–70
Table 4. Effect of Early Revascularization on Mortality
Odds Ratio for Death Revascularization Within 18 h of Shock vs. No/Late Revascularization
Odds
n Ratio 95% CI Comments
Trial 302 0.69 0.44, 1.08 152 randomly assigned to early
(30-Day mortality)* revascularization and 150 to
no early revascularization
Registry 753 0.37 0.27, 0.51 Unadjusted
(In-hospital mortality) 753 0.46 0.33, 0.66 Adjusted for age, diabetes,
MI to CS 6 h
353 0.58 0.35, 0.98 Adjusted for cardiac index and
age, diabetes, prior MI
*Trial in-hospital and 30-day mortality were similar.
CI Confidence interval.
larization in the Registry was 0.46, again roughly similar to Trial tertiary care centers had significantly lower mortality
the Trial OR of 0.69. than direct admissions to the SHOCK Trial centers. This is
attributed to the survival bias associated with transfer.
DISCUSSION Nevertheless, the mortality (67%) in the cohort with direct
admission remains lower than previous reports, perhaps
Major causes of CS. The relative incidence of the various
because of the increased utilization of IABP and revascu-
causes of CS has not been previously reported in a well-
larization. Although the mean LV ejection fraction was
defined large prospective study. The most frequent cause of
significantly lower for nonsurvivors, the 4% to 6% point
CS is predominant LV failure, most often with ECG
difference carries no clear clinical import with respect to
findings consistent with recent total coronary occlusion MI
patient stratification or pathophysiologic understanding.
with anterior location. Although inferior MI occurred often,
Outcome with thrombolysis and IABP. Patients selected
it was associated with prior MI in more than one-third of
to receive thrombolysis or IABP had lower mortality rates
the patients, or was associated with a mechanical cause of
shock. This supports the view that inferior MI alone than those not receiving those therapies, and the combina-
infrequently causes shock due to extensive LV dysfunction. tion appeared to be additive (14). Experimental evidence
Mechanical causes of CS, including VSR, acute severe suggests that the depressed rates of thrombus dissolution are
MR, and tamponade—all requiring early recognition and restored when IABP is used with thrombolysis in a hypo-
repair—accounted for 12% of cases. The mortality rate tensive model (23,24). Similarly, nonrandomized clinical
when VSR was the cause of shock was significantly higher studies have reported lower mortality for these combined
than that associated with other categories, emphasizing the therapies (25,26). Whether this combination is superior to
need for rapid septal repair before CS develops (16,17). It is thrombolysis alone for pump failure complicating acute MI
worth noting that the mortality rate associated with cardiac is being tested in the randomized Thrombolysis and Coun-
tamponade, which is often due to sub-acute cardiac rupture, terpulsation to Improve Cardiogenic Shock Survival Trial
was relatively low (18,19). This emphasizes the potential for (TACTICS) and How Effective are Revascularization Op-
improving survival with early detection. tions in Cardiogenic Shock Trial (HEROICS).
Patient profile. The characteristics of patients who de- PTCA and CABG. Previous studies, largely retrospective,
velop CS in the SHOCK Trial Registry are remarkably have demonstrated an association between the use of PTCA
similar to those in many other reports of CS (5,13,20 – or CABG and lower mortality (6 –10,27–34). The outcome
22). Patients with CS are often elderly and female and of revascularization performed at the SHOCK centers very
have high rates of prior MI, hypertension and diabetes. closely replicates the pooled rates from these studies. The
The timing of shock after MI onset, however, appears to mortality of LV failure patients undergoing PTCA at any
be markedly shorter than previously reported (5,13,20). time during the hospitalization for CS complicating acute
Whether this discrepancy results from the prospective MI is 45% for 646 patients in 22 studies (6 –10,27),
nature of a registry dedicated exclusively to CS or from a compared with 46% mortality for the 290 patients in the
change in the pathogenesis and/or the timing of CS is SHOCK Trial Registry. The 28% mortality rate for LV
unknown. failure patients undergoing CABG in our Registry is re-
Mortality. The overall mortality for patients with CS in markably similar to the pooled 35% mortality for 391
this SHOCK Trial Registry is 60%, which is lower than the patients in 25 studies undergoing CABG at any time during
80% to 90% rate in previous reports (21,22). This may be the hospitalization for CS (27–33). Furthermore, the out-
explained partly by the fact that 44% of the patients in the come with PTCA and CABG in the randomized SHOCK
SHOCK Trial Registry were transferred from community Trial was similar to these outcomes in the Registry (11).
hospitals. Not surprisingly, patients transferred to SHOCK Our observation that the mortality rate associated with
Downloaded from content.onlinejacc.org by on January 12, 2010

8. JACC Vol. 36, No. 3, Suppl A Hochman et al. 1069
September 2000:1063–70 CS Complicating Acute MI
revascularization is significantly lower than that associated Medical Center (Boston, MA); C. Buller, K. Gin, E.
with no revascularization is consistent with previous reports. Jamieson and R. Fox, Vancouver General Hospital (Van-
The patient characteristics of those clinically selected to couver, BC, Canada); D. H. Miller, T. Sanborn, R. Cam-
undergo revascularization are significantly different from pagna, O.Wayne Isom and S. Hosat, New York Hospital/
those not selected and explain a large part of the mortality Cornell Medical Center (New York, NY); H. White, J.
difference. In fact, the randomized SHOCK Trial demon- French, K. Graham and B. Williams, Green Lane Hospital
strated only 9% absolute and 17% relative mortality reduc- (Auckland, New Zealand); M. Menegus, M. Greenberg, R.
tion at 30 days (similar to the outcome at hospital discharge) Brodman and B. Levine, Montefiore/Albert Einstein Col-
for early revascularization, compared with initial medical lege of Medicine (Bronx, NY); J. Boland, R. Limet, S.
stabilization. The latter group often underwent IABP sup- Pourbaix, P. Baumans and M. Massoz, C.H.R. Citadelle
port and thrombolysis, and delayed revascularization was (Liege, Belgium); J. Col, R. Dion and R. Lauwers, Clin-
performed in 25% (11). The effect of early revascularization iques Universitaires St. Luc (Brussels, Belgium); R. For-
in the large Registry is somewhat greater than in the Trial
man, E. Scott Monrad, D. Sisto, M. Galvao and M. Jones,
after adjustment for differences in all characteristics except
J.D. Weiler Hospital of the Albert Einstein College of
for hemodynamics, which were available only in a subset.
Medicine (Bronx, NY); J. Ambrose, S. Sharma, T. Cocke,
After adjustment for the better hemodynamic profile of
J. Galla, D. Ratner and E. Brown, Mount Sinai Medical
those selected for revascularization, the effect of early
revascularization was similar in both the Trial and Registry. Center (New York, NY); R. Steingart and S. Parker,
It is possible that the small difference between ORs in favor Winthrop University Hospital (Mineola, NY); S. C. Wong,
of a greater benefit of early revascularization in the Registry, G. M. Gustafson, S. Papadakos, S. Lang, M. Brown and
compared with the Trial, is attributable to the more fre- M. Claude Boileau, New York Hospital Medical Center of
quent use of IABP and thrombolysis in the initial medical Queens (Flushing, NY); V. Dzavik, W. Tymchak, A.
stabilization arm of the Trial than in the Registry. Overall, Koshal, C. Kee and L. Harris, University of Alberta
the similarity of treatment effect in patients undergoing Hospital (Edmonton, Alberta, Canada); M. Porway, J.
revascularization in the Registry and Trial provides strong Flack and B. Burkott, Baystate Medical Center (Springfield,
support for the generalizability of the SHOCK Trial results MA); A. Moreyra, S. Palmeri, A. Spotnitz and M. Hosler,
to patients with CS complicating acute MI. Of note, the University of Medicine and Dentistry of New Jersey—
Trial reported increasing benefits of early revascularization Robert Wood Johnson Medical School (New Brunswick,
over time, with a large and significant mortality reduction at NJ); P. Aylward, J. Knight and C. Thomas, Flinders
six months consistent with 13 lives saved per 100 patients Medical Centre (Adelaide, SA, Australia); J. Dens, F. Van
treated (11). de Werf, P. Sergeants and C. Luys, Gasthuisberg University
In summary, the overall mortality for CS complicating Hospital (Leuven, Belgium); K. Baran, P. Koller, P. Filkins
acute MI in this international registry is lower than previ- and C. Iacarella, St. Paul Heart Clinic (St. Paul, MN); L.
ously reported, although CS due to VSR remains associated David Hillis, J. Cigarroa and J. Kissee, University of Texas
with very high mortality. This lower-than-expected mortal- SW Medical Center (Dallas, TX); S. Graham, S. Raza and
ity rate is likely due to higher revascularization rates in this J. Celano, Buffalo General Hospital (Buffalo, NY); J.
Registry, consistent with similar findings in a recent popu- Brinker and V. Coombs, Johns Hopkins Hospital (Balti-
lation study and randomized trial (11,35). more, MD); E. Ribeiro, A. Carlos Carvalho, C. Rodrigues
Alves and A. Petrizzo, Paulista School of Medicine (Sao
APPENDIX Paulo, Brazil); J. Dervan, W. Lawson and P.Montes, State
University of New York at Stony Brook (Stony Brook, NY);
The following are committee members, principal investiga-
D. Faxon and R. Singh, University of Southern California
tors and study coordinators in the SHOCK Study. Execu-
Medical Center (Los Angeles, CA); P. R. Paulsen and E.
tive Committee: J. Hochman, Study Chair; T. LeJemtel,
Miller, Hennepin County Medical Center (Minneapolis,
Co-chair; P. Aylward, J. Boland, J. Col, O. Wayne Isom, S.
McKinlay, M. Picard, T. Sanborn, L. Sleeper, H. White MN); B. Weiner and M. Borbone, University of Massa-
and P. Desvigne-Nickens (ex officio); Publications Com- chusetts (Worcester, MA); E. Bates, University of Michi-
mittee: H. White, Chair; J. Abel, J. Hochman, T. LeJemtel, gan Medical Center (Ann Arbor, myocardial Infarction);
L. Sleeper and J. Webb; Clinical Centers: J. Webb, C. Clinical Coordinating Center: J. S. Hochman, T. H.
Thompson, J. Abel and E. Buller, St. Paul’s Hospital LeJemtel and E. Godfrey, St. Luke’s/Roosevelt Hospital
(Vancouver, BC, Canada); J. David Talley, J. Harrell, M. Center (New York, NY); Data Coordinating Center: S. M.
Dearen, M. Rawert and R. Pacheco, University of Arkansas McKinlay, L. A. Sleeper, J. Lim and J. Nisbet-Brown, New
for Medical Sciences (Little Rock, AR); J. Slater, A. England Research Institutes (Watertown, MA); Program
Palazzo, R. Leber, C. Connery, and D. Tormey, St. Administration: P. Desvigne-Nickens, National Heart,
Luke’s–Roosevelt Hospital Center (New York, NY); A. Lung, and Blood Institute, National Institutes of Health
Jacobs, R. Shemin and M. Mazur, Boston University (Bethesda, MD).
Downloaded from content.onlinejacc.org by on January 12, 2010

9. 1070 Hochman et al. JACC Vol. 36, No. 3, Suppl A
CS Complicating Acute MI September 2000:1063–70
Acknowledgment 15. Wong SC, Lange RA, Webb J, et al. Intraaortic balloon counterpul-
sation enhances coronary thrombolysis induced by intravenous admin-
We acknowledge the American Heart Association, New
istration of a thrombolytic agent. J Am Coll Cardiol 1994;23;794 – 8.
York Affiliate for Grant-in-Aid support for the early phase 16. Ryan TJ, Anderson JL, Antman EM, et al. ACC/AHA Guidelines for
of the SHOCK Study. We thank the dedicated SHOCK the management of patients with acute myocardial infarction. J Am
investigators and coordinators for their outstanding perfor- Coll Cardiol 1996;28:1328 – 428.
17. Menon V, Webb JG, Hillis LD, et al., for the SHOCK Investigators.
mance and Dr. Patrice Desvigne-Nickens for her valuable Outcome and profile of ventricular septal rupture with cardiogenic
contribution to the Registry. shock after myocardial infarction: a report from the SHOCK Trial
Registry. J Am Coll Cardiol 2000;36:1110 – 6.
Request reprints and correspondence: Dr. Judith S. Hochman, 18. Lopez-Sendon J, Gonzalez A. Lopez de Sa E, et al. Diagnosis of
St. Luke’s Roosevelt Hospital Center, 1111 Amsterdam Avenue, subacute ventricular wall rupture after acute myocardial infarction:
sensitivity and specificity of clinical, hemodynamic, and echocardio-
New York, New York 10025. graphic criteria. J Am Coll Cardiol 1992;19:1145–53.
19. Slater J, Brown RJ, Antonelli TA, et al., for the SHOCK Investiga-
tors. Cardiogenic shock due to cardiac free wall rupture or tamponade
REFERENCES after myocardial infarction: a report from the SHOCK Trial Registry.
J Am Coll Cardiol 2000;36:1117–22.
1. Gruppo Italiano Per Lo Studio Della Streptochinasi Ne’ll Infarto 20. Hands ME, Rutherford JD, Muller JE. The in-hospital development
Miocardico (GISSI). Effectiveness of intravenous thrombolytic treat-
of cardiogenic shock after myocardial infarction: incidence, predictors
ment in acute myocardial infarction. Lancet 1986;397– 401.
of occurrence, outcome, and prognostic factors. The MILIS Study
2. ISIS-2 (Second International Study of Infarct Survival) Collaborative
Group. Randomized trial of intravenous streptokinase, oral aspirin, Group. J Am Coll Cardiol 1989;14:40 – 6.
both, or neither among 17,187 cases of suspected acute myocardial 21. Killip T, Kimball JT. Treatment of myocardial infarction in a coronary
infarction. ISIS-2. Lancet 1988;2:349 – 60. care unit. A two-year experience with 250 patients. Am J Cardiol
3. Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. Indica- 1967;20:457– 64.
tions for Fibrinolytic therapy in suspected acute myocardial infarction: 22. Goldberg RJ, Gore JM, Alpert J, et al. Cardiogenic shock acute
collaborative overview of early mortality and major morbidity results myocardial infarction. Incidence and mortality from a community-
from all randomized trials of more than 1000 patients. Lancet wide perspective, 1975 to 1988. N Engl J Med 1991;325:1117–22.
1994;343:311–22. 23. Prewitt RM, Gu S, Schick U, Ducas J. Intraaortic balloon counter-
4. Becker RC, Gore JM, Lambrew C, Weaver WD, Rubison RM, pulsation enhances coronary thrombolysis induced by intravenous
French WJ, Tiefenbrunn AJ, Bowlby LJ, Rogers WJ. A composite administration of a thrombolytic agent. J Am Coll Cardiol 1994;23:
view of cardiac rupture in the United States National Registry of 794 – 8.
Myocardial Infarction. J Am Coll Cardiol 1996;27:1321– 6. 24. Prewitt RM, Gu S, Garger PJ, Ducas J. Marked systematic hypoten-
5. Holmes DR Jr, Bates ER, Kleiman NS, Kleiman NS, Sadowski Z, sion depresses coronary thrombolysis induced by intracoronary admin-
Horgan JH, Morris DC, Califf RM, Berger PB, Topol EJ. Contem- istration of recombinant tissue-type plasminogen activator. J Am Coll
porary reperfusion therapy for cardiogenic shock: the GUSTO-I trial Cardiol 1992;20:1626 –33.
experience. The GUSTO-I Investigators. Global Utilization of Strep- 25. Stomel RJ, Rasak M, Bates ER. Treatment strategies for acute
tokinase and Tissue Plasminogen Activator for Occluded Coronary myocardial infarction complicated by cardiogenic shock in a commu-
Arteries. J Am Coll Cardiol 1995;26:668 –74. nity hospital. Chest 1994;105:997–1002.
6. Lee L, Bates ER, Pitt B, Walton JA, Laufer N, O’Neill WW.
26. Barron HV, Pirzada SR, Lomnitz DJ, Every NR, Gore JM, Chou
Percutaneous transluminal coronary angioplasty improves survival in
TM. Use of intra-aortic balloon counterpulsation in patients with
acute myocardial infarction complicated by cardiogenic shock. Circ
1988;78:1345–51. acute myocardial infarction complicated by cardiogenic shock (abstr).
7. Verna E, Repetto S, Boscarini M, Ghezzi I, Binaghi G. Emergency J Am Coll Cardiol 1998;31 Suppl A:135A.
coronary angioplasty in patients with severe left ventricular dysfunction 27. Hochman JS, Gersh BJ, Acute Myocardial Infarction: Complications.
or cardiogenic shock after acute myocardial infarction. Eur Heart J In: Topol EJ, editor. Textbook of Cardiovascular Medicine.
1989;10:958 – 66. Lippincott-Raven Publishers, Philadelphia 1998.
8. Moosvi AR, Khaja F, Villanueva L, Gheorghiade M, Douthat L, 28. Guyton RA, Arcidi JM, Jr, Langford DA, Morris DC, Liberman HA,
Goldstein S. Early revascularization improves survival in cardiogenic Hatcher CR, Jr. Emergency coronary bypass for cardiogenic shock.
shock complicating acute myocardial infarction. J Am Coll Cardiol Circ 1987;76:V22–7.
1992;19:907–14. 29. Bolooki H. Emergency cardiac procedures in patients in cardiogenic
9. Yamamoto H, Hayashi Y, Oka Y, et al. Efficacy of percutaneous shock due to complications of coronary artery disease. Circ 1989;79:
transluminal coronary angioplasty in patients with acute myocardial II37– 48.
infarction complicated by cardiogenic shock. Jpn Cir J 1992;56:815– 30. Phillips SJ, Zeff RH, Skinner JR, Toon RS, Grignon A, Kongtahworn
21. C. Reperfusion protocol and results in 738 patients with evolving
10. Hibbard MD, Holmes DR Jr, Bailey KR, Reeder GS, Bresnahan JF, myocardial infarction. Ann Thorac Surg 1986;41:119 –25.
Gersh BJ. Percutaneous transluminal coronary angioplasty in patients 31. Kirklin JK, Blackstone EH, Zorn GL, Jr, et al. Intermediate-term
with cardiogenic shock. J Am Coll Cardiol 1992;9:639 – 46. results of coronary artery bypass grafting for acute myocardial infarc-
11. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in tion. Circ 1985;72:II175– 8.
acute myocardial infarction complicated by cardiogenic shock. New 32. Subramanian VA, Roberts AF, Zema MJ, et al. Cardiogenic shock
Engl J Med 1999;341:625–34.
following acute myocardial infarction: late functional results after
12. Hochman JS, Sleeper LA, Godfrey E, et al., for the SHOCK
emergency cardiac surgery. NY State J Med 1980;80:947–52.
Investigators. SHould we emergently revascularize Occluded Coronar-
ies for cardiogenic ShocK: an international randomized trial of 33. Keon WJ. New therapeutic approaches to acute myocardial infarction
rmergency PTCA/CABG-Trial Design. Am Heart J 1999;137:313– (MI) and its size: the surgical approach. Avd Exp Med Biol 1977;82:
21. 394 –7.
13. The GUSTO Investigators. An International randomized trial com- 34. Hochman JS, Boland J, Sleeper LA, et al., and the SHOCK Registry
paring four thrombolytic strategies for acute myocardial infarction. Investigators. Current spectrum of cardiogenic shock and effect of early
N Engl J Med 1993;329:673– 82. revascularization on mortality: results of an international registry. Circ
14. Sanborn TA, Sleeper LA, Bates ER, et al., for the SHOCK Investi- 1995;91:873– 881.
gators. Impact of thrombolysis, aortic counterpulsation, and their 35. Goldberg RJ, Samad NA, Yarzebski J, Gurwitz J, Bigelow C, Gore
combination in cardiogenic shock: a report from the SHOCK Trial JM. Temporal trends in cardiogenic shock complicating acute myo-
Registry. J Am Coll Cardiol 2000;36:1123–9. cardial infarction. New Engl J Med 1999;340:1162– 8.
Downloaded from content.onlinejacc.org by on January 12, 2010

10. Cardiogenic shock complicating acute myocardial infarction—etiologies,
management and outcome: a report from the SHOCK Trial Registry
Judith S. Hochman, Christopher E. Buller, Lynn A. Sleeper, Jean Boland, Vladimir
Dzavik, Timothy A. Sanborn, Emilie Godfrey, Harvey D. White, John Lim, Thierry
LeJemtel, for the SHOCK Investigators
J. Am. Coll. Cardiol. 2000;36;1063-1070
This information is current as of January 12, 2010
Updated Information including high-resolution figures, can be found at:
& Services http://content.onlinejacc.org/cgi/content/full/36/3_Suppl_A/1063
References This article cites 30 articles, 17 of which you can access for free
at:
http://content.onlinejacc.org/cgi/content/full/36/3_Suppl_A/1063
#BIBL
Citations This article has been cited by 39 HighWire-hosted articles:
http://content.onlinejacc.org/cgi/content/full/36/3_Suppl_A/1063
#otherarticles
Rights & Permissions Information about reproducing this article in parts (figures,
tables) or in its entirety can be found online at:
http://content.onlinejacc.org/misc/permissions.dtl
Reprints Information about ordering reprints can be found online:
http://content.onlinejacc.org/misc/reprints.dtl
Downloaded from content.onlinejacc.org by on January 12, 2010